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STEMI NSTEMI ST elevation depression ECG changes myocardial infarction
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ECG Changes in Acute Coronary Syndromes: STEMI & NSTEMI
Overview: Acute Coronary Syndromes (ACS)
ACS is classified based on two factors: coronary artery occlusion and ECG changes.
| Feature | STEMI | NSTEMI / Unstable Angina |
|---|---|---|
| Thrombus | Complete occlusion | Partial occlusion |
| ECG | ST elevation | ST depression / T-wave inversion / normal |
| Troponin | Positive (may be negative very early) | Positive (NSTEMI) / Negative (UA) |
The Physiology Behind ST Changes
Why does the ST segment move?
Severe acute ischemia lowers the resting membrane potential of affected myocytes and shortens their action potential duration. This creates a voltage gradient between normal and ischemic zones, generating currents of injury that shift the ST segment on the surface ECG.
- Transmural ischemia (full wall thickness) → ST vector points outward → ST elevation in overlying leads
- Subendocardial ischemia (inner layer only) → ST vector points inward toward cavity → ST depression in overlying leads (+ ST elevation in aVR)
(Harrison's Principles of Internal Medicine, 22e)
STEMI — ST-Elevation Myocardial Infarction
Definition
ST elevation in ≥2 contiguous leads caused by complete coronary occlusion → transmural ischemia and necrosis.
ECG Sequence (Evolution Over Time)
| Stage | Time | ECG Finding |
|---|---|---|
| Hyperacute | Minutes | Tall, peaked "hyperacute" T waves |
| Acute | Hours | ST elevation (convex/tombstone morphology) |
| Evolving | Hours–days | ST elevation + pathological Q waves develop |
| Subacute | Days–weeks | ST normalises; T-wave inversions appear |
| Chronic/Old | Weeks–months | Persistent Q waves; T waves may normalise |
Key ECG Features
- ST elevation: ≥1 mm in limb leads, ≥2 mm in precordial leads
- Morphology: Convex ("tombstone") upward curve — not concave
- Reciprocal ST depression: in leads 180° opposite the infarct territory
- Q waves: pathological if >40 ms wide or >25% of R-wave height
- aVR elevation: global subendocardial ischemia / left main disease
🫀 Anterior STEMI (LAD occlusion)
Massive ST elevation in V1–V3 ("tombstoning"), with reciprocal ST depression in inferior leads (II, III, aVF). Classic proximal LAD occlusion.
🫀 Anterolateral STEMI (proximal LAD)
ST elevation in V1–V6, I, aVL + hyperacute T waves V2–V4 + reciprocal depression in II, III, aVF.
🫀 Inferior STEMI (RCA or LCx occlusion)
ST elevation in II, III, aVF + reciprocal depression in I, aVL + posterior changes (tall R and ST depression in V1–V3).
Lead Localisation of STEMI
| Territory | Leads with ST Elevation | Artery |
|---|---|---|
| Anterior | V1–V4 | LAD (proximal) |
| Anterolateral | V1–V6, I, aVL | LAD (proximal) |
| Lateral | I, aVL, V5–V6 | LCx or diagonal |
| Inferior | II, III, aVF | RCA (usually) or LCx |
| Posterior | Tall R + ST depression V1–V3 | RCA or LCx |
| Right ventricle | V1, V3R–V4R | Proximal RCA |
NSTEMI — Non-ST-Elevation MI
Definition
Partial coronary occlusion → subendocardial ischemia. Troponin is elevated (differentiating from unstable angina, where troponin is negative).
ECG Features
- ST depression: ≥0.5 mm, horizontal or downsloping (more specific than upsloping)
- T-wave inversion: often deep, symmetric, most prominent in the territory of the affected artery
- Wellens' Sign: deep symmetric T-wave inversions in V2–V4 → critical LAD stenosis (high-risk NSTEMI equivalent)
- ECG may be normal in 30–40% of NSTEMI cases — diagnosis depends on troponin
Differentiating ST Depression Morphologies
| Morphology | Significance |
|---|---|
| Horizontal/downsloping | High specificity for ischemia |
| Upsloping | Lower specificity; can be normal variant |
| Downsloping with T inversion | Strongly suggests significant ischemia |
Differential Diagnosis of ST Elevation (not all STEMI!)
| Cause | Clue |
|---|---|
| Acute pericarditis | Diffuse saddle-shaped elevation + PR depression; involves all leads |
| Early repolarization | Young patients, concave ST elevation, J-point notch |
| LBBB | Wide QRS, discordant ST-T changes |
| Brugada syndrome | Coved ST elevation in V1–V2, RBBB-like |
| Takotsubo syndrome | Post-stress, anterior ST changes, apical ballooning |
| Hyperkalemia | Peaked T waves, wide QRS |
| LV aneurysm | Persistent ST elevation weeks after MI |
(Goldman-Cecil Medicine; Harrison's 22e)
Management Principle
The ECG distinction is immediately actionable:
- STEMI → Emergency reperfusion within 90 minutes (primary PCI) or 30 minutes (thrombolysis if PCI unavailable)
- NSTEMI → Anticoagulation, antiplatelets, risk-stratified PCI (usually within 24–72 hours)
ECG should be obtained within 10 minutes of arrival for any patient with chest pain. If initial ECG is non-diagnostic, repeat in 5–10 minutes. — Textbook of Family Medicine, 9e
Sources: Harrison's Principles of Internal Medicine 22e | Goldman-Cecil Medicine | Textbook of Family Medicine 9e
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